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PANCE Practice > PANCE Prep- Cardiology > Flashcards

PANCE Prep- Cardiology Flashcards

1
Q

In the bradycardia algorithm, if there is a pulse and the pt is unstable (Hypotension, AMS, refractory CP, acute HF, or symptomatic, what do you do?

A
  1. Give Atropine (1st line)
  2. if atropine not effective:
    - Epi infusion
    - Dopamin infusion
    - -Transcutaneous pacing

*there are 3 exceptions to symptomatic/unstable bradycardia

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2
Q

What are the exception to symptomatic/unstable bradycardia rule:

A
  1. 3rd degree heart block or AV dissociation: transcutaneous pacing usually 1st line* followed by permanent pacemaker as definitive tx
  2. BBs: metoprolol, esmolol, propranolol
  3. CCB: non-dihydropyridines* verapamil, diltiazem
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3
Q

What are the only 2 shockable rhythms using defibrillation (unsynchronized cardioversion)

A
  1. Ventricular fibrillation

2. Pulseless VT

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4
Q

In the tachycardia algorithm, what do you do if a person has a pulse but is unstable?

A
  • Unstable tachyarrhythmia
    1. Synchronized cardioversion
  1. if regular, narrow QRS complex, may consider Adenosine
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5
Q

Describe what you check for in the tachycardia algorithm and what you do?

A
  1. Check pulse
  2. if yes, Stable or unstable?
    - if unstable–> synchronized cardioversion
  3. if stable, is there a wide QRS 0.12 sec or more?
    - If yes (Wide QRS complex tachycardia)–> antiarrhythmic med: amiodarone, lidocaine or procainamide
    - If no (narrow QRS complex tachycardia-> vagal maneuvers, adenosine**, BB or CCB
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6
Q

What are the 3 important exceptions to stable tachyarrhythmia rule?

A
  1. atrial flutter: BB or CCB 1st line (skip adenosine)
  2. afib: BB or CCB 1st line (skip adenosine even though Aflutter is often regular and narrow QRS)
  3. Wolff-Parkinson-White: Procainamide preferred** or amiodarone- avoid use of AV nodal blockers
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7
Q

What med do you usue if you have a regular and narrow QRS tachyarrhythmia?

A

adenosine

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8
Q

What meds should you avoid in WPW and why?

A

AV nodal blockers (ABCD)

  • Adenosine
  • BB
  • CCB
  • Digoxin

*AV nodal blockade may cause preferential conduction through the fast (preexcitation) pathway–> worsening of the tachyarrhythmia

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9
Q

Describe interpreting an EKG

A
  1. Determine rhythm (R-R regular?)
  2. Rate: (300-150-100-75-60-50) or #r waves in 6 second strip x10
  3. QRS axis deviation?
  4. P for every QRS
  5. PR interval?
  6. QRS interval?
  7. LBBB or RBBB?
  8. RVH or LVH?
  9. Pathological Q waves: >1 box in depth or height or prolonged QT?
  10. ST depression or elevation: >1mm
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10
Q

Describe the normal intervals
PR:
QRS:
QT:

Small box:
Big box:

A

PR: 3-5 small boxes (0.12-0.2sec)
QRS: <3 small boxes (<0.12 sec)
QT: 7.5-11 small boxes (0.3-0.44 sec)

Small box:
Big box:

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11
Q

Describe the sympathetic NS control of the heart

A

Hormones Epi and NE cause

  1. increased excitability
  2. increased force of contraction
  3. increased SA node discharge rate (increase HR)

*Epi and dobutamine are sympathomimetics (stimulate the SNS)

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12
Q

Describe the parasympathetic NS control of the heart

A

Hormone acetylcholine (regulated by the vagus nerve) causes:

  1. decreased excitability
  2. decreased force of contraction
  3. decreased SA node discharge rate (decrease HR)
  • Vagal stimulation or vagal maneuvers slow down the HR
  • Conversely, anticholinergic drugs increase the HR
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13
Q

How do you determine LBBB or RBBB

A

LBBB:

  1. Wide QRS >0.12sec
  2. Broad, slurred/bunny ears bumps R in V5,6
  3. Deep S wave in V1
  4. ST elevation in V1-V3

RBBB:

  1. Wide QRS >0.12sec
  2. RsR’ in V1, V2
  3. Wide S wave in V6
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14
Q

Describe the leads involved and artery involved for the area of infarction:

Anterior wall

A

V1-V4 (V3,4*)–Q waves/ ST elevation

LAD artery or LCA

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15
Q

Describe the leads involved and artery involved for the area of infarction:

Septal

A

V1 and V2– Q waves/ ST elevation

Proximal LAD

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16
Q

Describe the leads involved and artery involved for the area of infarction:

Lateral wall

A

I, aVL, V5, V6– Q waves/ ST elevation

Left circumflex artery

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17
Q

Describe the leads involved and artery involved for the area of infarction:

Anterolateral

A

I, aVL, V4, V5, V6– Q waves/ ST elevation

Mid LAD or LCX

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18
Q

Describe the leads involved and artery involved for the area of infarction:

inferior

A

II, III, aVF– Q waves/ ST elevation

RCA

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19
Q

Describe the leads involved and artery involved for the area of infarction:

Posterior Wall

A

V1-V2 ST Depression**

RCA or LCX

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20
Q

What is a normal QRS axis

A
  • 30 to +90 degrees

* look at leads I and aVF (use hands)

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21
Q

LAD vectors move towards ___ or away from ____

RAD vectors more towards ___ or away from ____

A

LAD: towards LVH or away from infarction (inferior MI +/- cause LAD)

RAD: towards RVH or away from infarction (lateral MI +/- cause RAD)

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22
Q

Causes of Left axis deviations

A
  1. LBBB
  2. LVH
    3 Inferior MI
  3. Elevated diaphragm
  4. L anterior hemiblock
  5. WPW
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23
Q

Causes of right axis deviations

A
  1. RVH
  2. Lateral MI
  3. COPD
  4. Left posterior hemiblock
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24
Q

in NSR, P waves are positive/upright in leads:___ and neg in leads: ___

A

Positive P: I, II, aVF

Negative P: aVR

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25
Q

Pathologic causes of bradycardia and what is the 1st line tx

A
  1. BB
  2. CCB
  3. Digoxin
  4. carotid massage
  5. SA node ischemia
  6. Gram Neg. sepsis
  7. hypothyroidism

*Anticholinergic Atropine is 1st line (bc excess vagal stimulation is the MC cause of bradycardia)

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26
Q

Heart rate typically ___ during inspiration

A

Increases in inspiration

decreases in expiration

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27
Q

What is sick sinus syndrome

A

Brady-tachy syndrome

  • Combination of sinus arrest w/ alternating pparoxysms of atrial tachyarrhythmias and bradyarrhythmias
  • commonly caused by SA node disease and corrective cardiac surgery
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28
Q

Management of Sick Sinus Syndrome

A
  1. Permanent pacemaker if symptomatic (dual chamber pacing usually preferred over ventricular pacing).
  2. *if brady alternating with ventricular tachycardia–> permanent pacemaker w/ automatic implantable cardioverter-defibrillator (AICD)
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29
Q

___ is the most helpful in determining the presence of AV conduction blocks

A

PR interval

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30
Q

Describe 1st, 2nd type 1 and 2, and 3rd degree AV blocks

A

1st: Fixed, prolonged PRI (>0.2sec) and QRS followed by every P

2nd Type I (Wenckebach): Progressive PRI lengthening then DROPPED QRS

2nd Type II (Mobitz II): Fixed prolonged PRI then DROPPED QRS

3rd: AV dissociation: P waves NOT related to QRS, all P waves NOT followed by QRS = decreased Cardiac output

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31
Q

What is the management of 1st, 2nd type 1 and 2, and 3rd degree AV blocks

A

1st: none, observe (may progress)

2nd type I (Wenckebach):

  • Symptomatic: ATROPINE, epi +/- pacemaker
  • Asymptomatic: observe +/- cardiac consult

2nd type II: ATROPINE OR TEMP. PACING, (progression to 3rd degree is common so PPM is definitive tx)

3rd:
- Acute/symptomatic: temporary pacing–> PPM
- Definitive tx: PPM

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32
Q

Describe the appearance of Aflutter

A
  1. “saw tooth” waves

2. Rate: 250-350bpm (no P waves but is usually REGULAR)

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33
Q

Management of Atrial flutter

A
  1. Stable: Vagal, BB, or CCB
  2. Unstable: Direct current synchronized cardioversion
  3. Definitive tx: Radiofrequency ablation

*Anticoagulation use is similar to afib

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34
Q

___ is the most common chronic arrhythmia

A

atrial fibrillation

*most patients are asymptomatic

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35
Q

Why are people with atrial fibrillation at increase risk for stroke?

A

The ineffective quivering of the atria may cause thrombi (clots) to form, which can embolize and cause ischemic strokes

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36
Q

Etiologies of Afib

A
  1. Cardiac disease
  2. Ischemia
  3. pulmonary disease
  4. infection
  5. cardiomyopathy
  6. electrolyte/hormone imbalance (hypothyroidism)
  7. Idiopathic- age, genetics, hemodynamic stress, meds, alcohol
  8. Men> women
  9. white>black
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37
Q

Describe the different types of Afib

A
  1. Paroxysmal: self terminating w/in 7 days (usually <24hrs) +/- recurrent
  2. Persistent: fails to self terminate, lasts >7 days (requires termination via medical or electrical)
  3. Permanent: persistent AF >1yr (refractory to cardioversion or cardioversion never tried)
  4. Lone: paroxysmal, persistent or permanent w/o evidence of heart disease
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38
Q

Management of Stable AFib

A
  1. Rate control (usually preferred as initial management of symptomatic AF over rhythm control)
    - BB: Metoprolol (cautious use in those w/ reactive airway dz**)
    - CCB: Diltiazem*, verapamil (non-dihydropyridines)
    - Digoxin: +/- use in elderly, **Preferred for rate control in pts w/ hypotension or CHF (not generally used in active patients)
  2. Rhythm control
    - Direct current synchronized cardioversion (DCC):
    - Pharmacologic: Ibutilide, Flecainide, Sotalol, Amiodarone
    - Radiofrequency ablation: PPM, cath-based ablation or surgical MAZE procedure
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39
Q

Direct current (synchronized) cardioversion (DCC) can be done for AFib if:

A
  1. AF present >48 hrs OR
  2. After 3-4 weeks of anticoagulation and a transesophageal echocardiogram (TEE) shows no atrial thrombi OR
  3. Start IV heparin, cardiovert w/in 24 hrs and anticoagulation for 4 weeks
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40
Q

Management of unstable Afib

A

Direct current synchronized cardioversion (DCC)

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41
Q

All patients with non-valvular Afib should undergo:

A
  1. assessment of the risk of embolization via CHAD2DS2-VASc or CHADS2
    * shown to reduce embolic risk by 70%
  2. Determination benefits vs risks of anticoagulation via clinical judgment and discussion w/ patient
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42
Q

Describe the CHA2DS2-VASc Scoring Criteria for afib

A
  1. CHF: 1
  2. HTN: 1
  3. Age 75 or older: 2
  4. DM: 1
  5. S: Stroke, TIA, thrombus hx: 2
  6. V: Vascular dz (prior MI, aortic plaque, PAD): 1
  7. A: Age 65-74: 1
  8. S: Sex: female: 1

-2 or more= moderate to high risk= chronic oral anticoag. recommended
-1= low risk= consider risks/benefits
0= very low risk= no anticoag. needed

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43
Q

Describe the CHADS2 Scoring Criteria for afib

A
  1. C: CHF: 1
  2. H: HTN: 1
  3. A: Age: 75 or older: 1
  4. D: DM: 1
  5. S: Stroke, TIA, thrombus hx: 2
  • 2 or more= high risk: Warfarin
  • 1= moderate risk: warfarin or ASA
  • 0= low risk: non or ASA
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44
Q

Describe types of anticoagulant agents

A
  1. Non-vitamin K antagonist oral anticoagulants (NOAC): usually now preferred over warfarin in most cases due to similar or lower rates of major bleedig and less DDI and less drug monitoring
    - Dabigatran: direct thrombin inhibitor
    - Rivaroxaban, Apixaban, Edoxaban: factor Xa inhibitors
  2. Warfarin:
  3. Dual Antiplatelet therapy: ASA + clopidogrel (anticoagulant monotherapy is superior to dual antiplatelet therapy)
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45
Q

What are Factor Xa inhibitors?
What are direct thrombin inhibitors?

Describe their MOA

A

Factor Xa inhibitors: Rivaroxaban (Xarelto), Apixiban (Eliquis), Edoxaban (Savaysa)–> selectively binds to antithrombin III)

Direct thrombin inhibitors: Dabigatran (Pradaxa)–> binds and inhibits thrombin

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46
Q

What are some contraindications to NOAC? (non-vitamin K antagonist oral anticoagulants)

A
  1. Severe chronic kidney disease
  2. HIV pts on potease inhibitor-based therapy
  3. on CP450 inducing antiepileptic meds such as carbamazepine, phenytoin,
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47
Q

What are common causes of prolonged QT syndrome and common clinical manifestations

A

congenital or acquired

  1. Macrolides
  2. TCA
  3. electrolyte abnormalities
  4. recurrent syncope,
  5. Ventricular arrythymias
  6. sudden cardiac death
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48
Q

Management of Prolonged QT Syndrome

A
  1. DC offending drug and correct electrolyte abnormalities

2. AICD if definitive tx for congenital or recurrent ventricular arrhythmias

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49
Q

What rhythm?

  • HR >100
  • Regular rhythm with narrow QRS
  • P waves hard to discern due to rapid rate
A

(p)SVT

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50
Q

Describe the 2 main types of pSVT

A
  1. AVNRT: AV nodal reentry tachycardia: 2 pathways both within the AV node (slow and fast) **MC TYPE
  2. AVRT: AV Reciprocating tachycardia: 1 pathway within the AV node and a second accessory pathway OUTSIDE the AV node ex. WPW and LGL
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51
Q

Describe the conduction patterns that result in Narrow complex tachycardia and wide complex tachycardia

A

Narrow complex tachy: Orthodromic (95%): Impulse goes down the normal AV node pathway first and returns via the accessory pathway in circles, perpetuating the rhythm

Wide complex tachy: Antidromic (5%): Impulse goes down the accessory pathway first and returns to the atria via the normal pathway (mimics VT)

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52
Q

Management of Stable Narrow Complex SVT vs Stable Wide complex SVT

A

Narrow Complex SVT:

  1. Vagal maneuvers (vagus nerve stimulation releases acetylcholine = decrease HR)
  2. Adenosine 1st line medical tx for SVT (terminates 90% of narrow complex SVT) **may cause bronchospasm for those w/ asthma/COPD
  3. AV nodal blockers: BB or CCB

Wide Complex SVT:
1. Antiarrhythmics: ex. Amiodarone or Procainamide if WPW

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53
Q

Tx of unstable SVT (wide or narrow complex) and what is the definitive tx of SVT

A
  1. direct current synchronized cardioversion

Definitive: Radiofrequency ablation

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54
Q

What rhythm?

  • HR <100 and
  • 3 or more P wave morphologies
A

Wandering atrial pacemaker: multiple ectopic atrial foci generated impulses that are conducted to the ventricles

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55
Q

What rhythm?

  • HR >100 and
  • 3 or more p wave morphologies
A

Multifocal atrial tachycardia

*same as WAP but HR is >100

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56
Q

Multifocal Atrial Tachycardia (MAT) is commonly associated with ___ and is difficult to tx but usually use: ___

A

Severe COPD

Tx: CCB (Verapamil) or BB if LV fxn presereved

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57
Q

What EKG findings are associated w/ WPW and what is WPW

A
  1. Delta wave (slurred QRS upstroke)
  2. Wide QRS (>0.12sec)
  3. Short PRI

*accessory pathway (bundle of Kent) pre-excites the ventricles–> a type of of AVRT

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58
Q

Management of

  • Stable WPW
  • Unstable WPW
  • Definitive management
A
  1. Vagal maneuver
  2. Antiarrhythmics ex. Class IA: Procainamide preferred***, amiodarone, flecainide
  3. Avoid the use of AV nodal blockers (ABCD) in WPW**

Unstable: direct current synchronized cardioversion

Definitive: radiofrequency ablation

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59
Q

What rhythm?

  • Short PRI
  • Normal QRS complex
A

Lown-Ganong-Levine Syndrome (LGL)

*type of AVRT leading to a short PRI) but the accessory pathway (bundle of james) connects to the bundle of HIS so the QRS is narrow in LGL (unlike the wide QRS in WPW)

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60
Q

What Rhythm?

  • Regular rhythm
  • P waves inverted (negative) if present in leads where they are normally positive (I, II, aVF) or are not seen
  • Classical associated w a narrow QRS
A

AV junctional dysrhythmias

*AV node/junction becomes the dominant pacemaker of the heart

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61
Q

MC rhythm seen w/ digitalis toxicity

A

AV junctional dysrhythmia

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62
Q

What are the 3 types of AV junctional dysrhythmias

A
  1. Junctional rhythm: HR 40-60,
  2. Accelerated Junctional: HR 60-100
  3. Junctional tachycardia: HR >100
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63
Q
  • Wide, bizarre QRS occurring earlier than expected.
  • The T wave is in the opposite direction of the QRS usually
  • Associated w a compensatory pause
A

PVC

*no tx usually needed

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64
Q

Ventricular tachycardia is considered:

A

3 or more consecutive PVCs at a rate >100bpm

-Sustained VT= lasting 30 or more seconds

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65
Q

___ is a common predisposing condition for VT

A

Prolonged QT interval

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66
Q

Torsades De Pointes is most commonly due to ___

A

hypomagnesemia, hypokalemia

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67
Q

Management of the following VTs:

  1. Stable sustained VT
  2. Unstable VT w/ a pulse
  3. Pulseless VT
  4. Torsades de pointes:
A
  1. Stable sustained VT: Antiarrhythmics (amiodarone, lidocaine)
  2. Unstable VT w/ a pulse: Synchronized cardioversion
  3. Pulseless VT: defibrillation (unsynchronized cardioversion) + CPR (tx as VF)
  4. Torsades de pointes: IV magnesium
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68
Q

Management of VF

A

Unsynchronized cardioversion (defibrillation) + CPR

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69
Q

Management of PEA (pulseless electrical activity) or asystole

A
  1. CPR
  2. Epi
  3. Checks for “shockable” rhythms every 2 min
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70
Q 
Causes of increased jugular pressure
Increased JVP + \_\_\_\_ = \_\_\_\_
1. + Crackles/rales 
2. + Normal pulmonary exam
3. + decreased breath sounds
A
    • Crackles/rales: CHF
    • Normal pulmonary exam: Pericardial (tamponade or constrictive pericarditis)
    • decreased breath sounds: Tension pneumothorax
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71
Q

Causes of ST Elevation

A
  1. Acute MI
  2. LVH
  3. LBBB
  4. Acute pericarditis
  5. Early repolarization abnormalities
  6. Coronary vasospasm/Prinzmetal angina/cocaine
  7. Brugada syndrome
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72
Q

EKG findings with pericarditis

A
  1. Diffuse concave ST elevation in precordial leads (V1-V6)
  2. PR depression in same leads w/ ST elevation
  3. in aVR: ST depression and PR elevation
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73
Q

EKG signs of LVH w/ LV strain

A
  1. ST elevation in right precordial leads (V1-V3)
  2. Increase voltage
  3. Asymmetric ST depressions and T wave inversions in the lateral leads (I, aVL, V5, V6)
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74
Q

Describe Brugada Syndrome EKG patterns

A
  1. RBBB (often incomplete) in V1-V3
  2. ST elevation V1-V3 (often downsloping)
  3. T wave inversion in V1 and V2
  4. +/- S wave in lateral leads (I, aVL, V5, V6)
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75
Q

Brugada Syndrome is

  1. MC in ___
  2. Associated with ___
  3. Often caused by: ___
  4. Management includes: ___
A
  1. MC in Asian Males
  2. Associated w/ syncope and sudden cardiac death from ventricular arrhythmias
  3. Often caused by genetic disorder
  4. Managed w/ AICD to prevent death from VF
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76
Q

Kussmaul’s sign is an increase rather than the normal decrease in the CVP during inspiration. It is most often caused by

A
  1. severe right-sided heart failure;
  2. constrictive pericarditis or
  3. right ventricular infarction.
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77
Q

A 25 year-old female presents with a three-day history of chest pain aggravated by coughing and relieved by sitting. She is febrile and a CBC with differential reveals leukocytosis. Which of the following physical exam signs is characteristic of her problem?

A

Pericardial friction rub- pericarditis

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78
Q

A 22 year-old male received a stab wound in the chest an hour ago. The diagnosis of pericardial tamponade is strongly supported by the presence of

A

distended neck veins- Cardiac compression will manifest with distended neck veins and cold clammy skin

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79
Q

What test is done to detect ventricular wall dysfunction

A

Cardiac nuclear scanning

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80
Q

PT-INR is a reflection of the ___ pathway clotting system. Coumadin interferes with Vitamin K synthesis which is needed in the manufacture of factors ___ which are part of that clotting pathway

A

extrinsic and common

factors II, VII, IX, X
2,7,9,10 (1972- Extrinsic)

81
Q

What antiarrhythmic drugs can be associated with hyper- or hypothyroidism following long-term use?

A

amiodarone

82
Q

What hypertensive emergency drugs has the potential for developing cyanide toxicity?

A

Sodium nitroprusside metabolization results in cyanide ion production. It can be treated with sodium thiosulfite, which combines with the cyanide ion to form thiocyanate, which is nontoxic

83
Q

What beta-adrenergic blocking agents has cardioselectivity for primarily blocking beta-1 receptors?

A

Metoprolol

84
Q

Describe the mechanisms of the following classes of antiarrhythmic drugs:

  1. Class I:
  2. Class II:
  3. Class III:
  4. Class IV:
A
  1. Class I: Na+ channel blockade
  2. Class II: Beta-adrenergic receptor blockade, BB
  3. Class III: K+ channel blockers
  4. Class IV: Ca channel blockade, CCB
85
Q
  1. Atrial contraction against a noncompliant ventricle is the mechanism responsible for ___
  2. Rapid ventricular filling during early diastole is the mechanism responsible for __
  3. Vibration of a partially closed mitral valve during mid to late diastole is the mechanism responsible for ____.
  4. Closure of the mitral valve leaflets during systole is the mechanism responsible for part of ___
A
  1. S4
  2. S3 gallop
  3. aortic regurgitation- the Austin-Flint murmur of AR
  4. S1
86
Q

___ is the most common cause of secondary hypertension.

A

Renal parenchymal disease

87
Q

What medication classes is the treatment of choice in a patient with variant or Prinzmetal’s angina?

A

CCB

*BB have been noted to exacerbate coronary vasospasm potentially leading to worsening ischemia.

88
Q

What is the EKG manifestation of cardiac end-organ damage due to hypertension?

A

LVH

89
Q

Periodic measurements of blood pressure should be part of routine preventive health assessments beginning at the age of __

A

3 years.

90
Q

____ is characterized by a medium- pitched, mid-systolic murmur that decreases with squatting and increases with straining.

A

Hypertrophic cardiomyopathy

91
Q

EKG Pattern:

  1. (incomplete) RBBB in V1-V3
  2. ST elevation V1-V3 (often downsloping)
  3. T wave inversion in V1 and V2
  4. +/- S wave in lateral leads (I, aVL, V5, V6)
A

Brugada syndrome

92
Q

How do vagal maneuvers and carotid massage decrease HR in tachycarrhythmias?

A

baroreceptors sense increase carotid artery pressure–> reflexive decrease in HR

93
Q

What is the equation for cardiac output

A

CO= SV X HR

94
Q

What sounds make up S1 and S2

A

S1: closing of mitral and tricupsid valves
S2: closing of aortic and pulmonic valves

95
Q

What is pulsus paradoxus and when is it seen?

A

> 10mmHg decline in SB with inspiration (palpable peripheral pulses disappear w/ inspiration)

EX: Cardiac tamponade and tension pneumothorax

96
Q

Cautious use w/ IV nitro and morphine with what types of MIs and why?

A

R-sided and inferior MIs

-Bc right side is more dependent on preload and SV to maintain CO and nitro and morphine decreases preload

97
Q

Describe how BP is controlled

A

Renin-Angiotensin-Aldosterone System
-low BP–> renin release by kidneys–> renin+ angiotensinogen= angiotensin I–> cleaved by ACE from lungs= angiotensin II–> increases BP

Angiotensin II Effects:

  • increase aldosterone= increase Na retention (K+ and H+ secretion)
  • Increase ADH= H20 retention
  • Vasoconstriction= increase BP
  • Increase sympathetic tone= increase BP
98
Q

SE of ACE inhibitors and why

A
  1. can cause hyperkalemia bc they inhibit aldosterone which typically increases K+ excretion
  2. Cough or angioedema bc they potentiate other vasodilators (ex. bradykinin)

*ARBs (angiotensin II receptor blockers) block the receptor for AGII but don’t cause angioedema or cough

99
Q

What drugs are used for pharmacologic stress testing and when is this contraindicated

A

Vasodilators: adenosine or dipyridamole (dobutamine is 2nd line)
*localizes region of ischemia

CI: bronchspastic disease

100
Q

Risk factors for CAD

A
  1. DM (worst)
  2. Cig smoking
  3. Hyperlipidemia
  4. HTN
  5. Age (M >45, F>55)
  6. FHX
101
Q

Describe the pathophysiology of atherosclerosis

A
  1. Fatty streak formation: lipid deposition in WBC–> smooth muscle proliferation (forms streaks)
  2. LDL enters endothelium in the fatty streaks and LDL becomes oxidized which attracts other WBCs
  3. proliferating smooth muscle cells and CT makes “fibrous cap” and arterial lumen narrowing +/- calcification (stabilized plaque)
102
Q

Arterial lumen is typically ____% narrowed when a patient becomes symptomatic to myocardial ischemia w/ exertion and ____% narrowed when symptomatic at rest

A

70% or more narrowed w/ exertion

> 90% at rest

103
Q

What is angina pectoris

A

substernal CP usually brought on by exertion (due to decrease coronary blood supply and increased demand)

104
Q

Describe common features of cardiac CP

A
  1. substernal
  2. poorly localized
  3. exertional
  4. radiates to arm, teeth, lower jaw, back,
  5. typically 1-5 min
  6. relieved w/ nitro or rest
105
Q

Resting EKG is normal in __% of patients with stable angina

A

50%

106
Q

When is PTCA indicated for management of angina

A

1-2 vessel disease NOT involving LM and in whom LV fxn is normal/near normal
*restenosis is prevented with stents w/ drug-eluting properties

107
Q

Indications for CABG

A
  1. LM disease
  2. Symptomatic or critical stenotic 3-vessel disease (>70% stenosis)
  3. Decreased LV EF <40%
108
Q

What is the pharmacologic management of stable (chronic) angina

(and their MOA)

A
  1. Nitrates (vasodilates and increases O2 supply, reduces coronary spasm, and decreases demand by decreased preload venodilation)
  2. BB (increase O2 supply by prolonging coronary artery filling times/diastolic time, and decreased O2 demand) **1st line
  3. CCB (increase O2 suply and prevents ischemia induced coronary vasospasm*, decreased demand/contractility)
  4. ASA (prevents platelet activation/aggregation by inhibiting cyclooxygenase–> decreased thromboxane A2 and inhibit prostaglandins)

Typical Regimen: ASA + SL nitro PRN + BB + statin

109
Q

SE of Nitrates

And when are nitrates contraindicated

A
  1. HA
  2. flushing
  3. hypotension
  4. tachyphylaxis after 24 hrs

CI: SBP <90, RV infarction, Use of sildenafil and other PDE-5 inhibitors

110
Q

What medication is the 1st line drug for chronic management in stable (chronic) angina

A

Beta blockers - reduces mortality, symptoms and prevents ischemic occurrences)

111
Q

What BB are cardioselective (B1) and what ones are nonselective?

A

Selective (B1): Metoprolol and Atenolol

Nonselective: Propranolol, Nadolol

112
Q

What medication is indicated for prinzmetal angina?

A

CCB

nondihydropyridines: Diltiazem or verapamil (long acing)

113
Q

Who are most likely to suffer from a “Silent or atypical MI”

A
  1. women
  2. Elderly
  3. Diabetics
  4. obese

sx: abdominal pain, jaw pain, dyspnea w/o CP

114
Q

STEMI is defined as:

A
  1. ST elevations 1mm or more in 2 or more anatomically contiguous leads
  2. +/- reciprocal changes in opposite leads
  3. New LBBB is considered STEMI equivalent
115
Q

Cardiac markers for MI include:
-Standard is usually __ sets every ___

-describe when these markers appear, peak and return to baseline

A
  1. Troponin- most sensitive and specific**
    - appear 4-8hr
    - peaks: 12-24hr
    - Returns to baseline: 7-10 days
  2. CK/CK-MB
    - appear 4-6hr
    - peaks: 12-24hr
    - Returns to baseline: 3-4days

*3 sets q8hrs

116
Q

Management of unstable angina or NSTEMI

A

**ASA, Heparin, NTG, BB + (MONA- morphine, oxygen, nitro, ASA)
1. Antithrombotic therapy (anitplatelet + anticoagulant)
-ASA
-ADP inhibitors: clopidogrel
-GP IIb/IIIa inhibitors
Anticoags: (indicated for ECG changes or + cardiac markers)
-Unfractionated heparin
-LMWH (enoxaprin)
-Fondaparinux
2. Adjunctive anti-ischemic
-BB
-Nitrates
-Morphine
-CCB

117
Q

Compare the MOA of

  • Unfractionated heparin:
  • LMWH (enoxaparin):
  • Fondaparinux:
A

Heparin (UFHLMWH): inhibits thrombin by activating antithrombin III and inhibits factor Xa
- (LMWH more specific to Factor Xa than UFH)

-Fondaparinux: direct factor Xa inhibitors (binds to and enhances antithrombin)- no direct effects on thrombin

118
Q

Management of STEMI

A
  • *ASA, Heparin, REPERFUSION, ACEI, NTG, BB + (MONA- morphine, oxygen, nitro, ASA)
    1. Reperfusion (most important) w/in 12 ho urs of sx onset (PCI or thrombolytics w/ rTPA)
    2. Antithrombotics (ASA, heparin, Glycoprotein IIb/IIIa inhibitors)
    3. Adjunctive therapy
  • BB
  • ACEI- slows the progression of CHF by decreasing ventricular remodeling*
  • Nitrates
  • Morphine
  • Statin
119
Q

PCI is best w/in ___ hours of sx onset

A

3 hours (esp c/n 90min)

  • Door to thrombolyics: w/in 30 min
  • Door to PCI: w/in 90 mins (+/- 30min)
120
Q

Management of Cocaine-induced MI

A

ASA, Heparin, Nitro, anxiolytics (BENZOs), CCB

*AVOID BB bc of unopposed alpha vasoconstriction/vasospasm

121
Q

Describe what to do if someone presents w/ sx associated w/ ischemia or infarction

A
  1. brief hx and exam
  2. Cardiac markers
  3. MONA (morphine, O2 4L, Nitro, ASA)
  4. EKG w/in 10 min of entering ER
  5. PCI w/in 90 min or fibrinolysis w/in 30 min
122
Q

What is Dressler Syndrome

A
  1. post MI pericarditis
    • fever
    • pulmonary infiltrates
123
Q

What is variant (prinzmetal) angina and how is it diagnosed?

A

coronary spasm w/ transient ST elevations (usually w/o MI)

  • CP usually nonexertional, often at rest
  • DX: EKG +/- transient ST elevations
  • angiography vasospasm w/ IV Ergonovine administration

Sx and ST elevations resolve w/ CCB or nitro

124
Q

What is the drug of choice for variant (prinzmetal) angina?

A

CCB* and nitro PRN

125
Q

What is cocaine induced CP/MI?

A

coronary artery vasospasm due to cocaines activation of sympathetic nervous system and alpha-1 receptor–> vasoconstriction

126
Q

Most common cause of CHF

A

CAD

127
Q

What is the chief adverse effect of thiazide diuretics?

A

-hypokalemia**
Also causes
-hyponatremia
-retention of Ca++

128
Q

___ is classically described in children as a continuous machinery-type murmur that is widely transmitted across the precordium.

A

Patent ductus arteriosus

129
Q

___ leads to enlargement of the left atrium, which is the major predisposing risk factor for the development of atrial fibrillation.

A

Mitral stenosis

130
Q

__ and __ are the most common drugs that may cause a lupus-like eruption.

A

Procainamide and hydralazine

131
Q

Which electrolyte abnormality is associated with an increase in the risk for digoxin toxicity?

A

hypokalemia

*Decreased concentration of potassium results in the increased activity of cardiac glycosides by increasing tissue binding and decreasing renal excretion of digoxin. Potassium loss is the only significant electrolyte abnormality that significantly affects digoxin metabolism.

132
Q

___ is characterized by a holosystolic murmur at the lower left sternal border.

A

Ventricular septal defect

133
Q

___ is characterized by a systolic thrill at the left sternal border with a systolic ejection murmur that may or may not have an associated systolic click.

A

Tetralogy of Fallot

134
Q

__ is associated with a systolic ejection click or a short systolic murmur at the left sternal border.

A

Coarctation of the aorta

135
Q
  1. A grade IV/VI systolic murmur heard best at the apex with radiation to the left axilla
  2. A grade III/VI diastolic murmur heard best at the apex without radiation
  3. A grade IV/VI systolic ejection murmur heard best at the base with radiation to the left clavicle.
  4. A grade II/VI systolic murmur heard best at the apex preceded by a click and without radiation.
A
  1. MR
  2. MS
  3. pulmonic stenosis
  4. MV prolapse
136
Q

___ accounts for more than 60% of all cases of endocarditis in IV drug abusers.

A

S. aureus

137
Q

An electrocardiogram (ECG) shows a sinus rhythm with varying T wave heights, axis changes every other beat and a wandering baseline. Which of the following is most likely the diagnosis?

A

Pericardial effusion

  • electrical alternans`
138
Q

Who is most at risk for developing primary HTN

A

Black non-Hispanic adults have the highest risk of hypertension.

139
Q

What is the optimal INR for a patient with a mechanical mitral valve prosthesis on warfarin (Coumadin)?

A

2.5-3.5

140
Q

Coronary artery perfusion occurs primarily during __

A

diastole

141
Q

Pulmonary capillary wedge pressure indirectly measures which of the following?

A

left atrial filling pressure

142
Q

Causes of left sided heart failure

A
  1. CAD **
  2. HTN**
  3. Valvular dz
  4. cardiomyopathies
143
Q

Causes of Right sided heart failure

A
  1. Left sided heart failure**
  2. Pulmonary dz** (COPD, PHTN)
  3. Mitral stenosis
144
Q

What is the difference btwn systolic and diastolic HF

A

Systolic: decreased EF +/- S3 gallop. (MC form)
Diastolic: normal EF +/- S4 gallop = forced atrial contraction into a stiff ventricle (associated w/ normal cardiac size)

145
Q

Causes of systolic HF

A
  1. Post MI
  2. dilated cardiomyopathy
  3. myocarditis
146
Q

Causes of diastolic HF

A
  1. HTN
  2. LVH
  3. Elderly
  4. Valvular dz
  5. cardiomyopathies
  6. Constrictive pericarditis
147
Q

Compare and contrast diastolic and systolic HF

A

Diastolic: NORMAL/increased EF, THICK ventriular walls, SMALL LV chamber, +S4
(thick and stiff)

Systolic: DECREASED EF, THIN venticular walls, DILATED LV chamber, S3

148
Q

Describe the NY Heart Association Functional Class of Heart Failure

A

Class I: No sx or physical limitations
Class II: Mild sx (dyspnea or angina), slight limitation
Class III: sx w/ limitation w/ activity, comfortable at rest
Class IV: sx at rest w/ severe limitations

149
Q

Describe the pathophysiology of heart failure

A

Initial insult leads to **Increased Afterload, increased preload and/or decreased contractility (heart tries to compensate for a short term)
Compensation includes:
1. SNS activation
2. Myocyte hypertrophy/remodeling
3. RAAS activation: fluid overload, ventricular remodeling/hypertrophy===> CHF

150
Q

Clinical Manifestations of Left sided HF

A
  • *Increase pulmonary venous pressure from fluid backing up into the lungs
    1. Dyspnea (MC SX)
    2. Pulmonary congestions (rales, rhonchi)
    3. Pink frothy sputum w/ nonproductive cough
    4. HTN
    5. Cheyne-Stokes breathing (deepr faster w/ gradual decrease and peroids of apnea)
    6. S3 (SHF) or S4 (DHF)
    7. Increased adrenergic activation (dusky, pale, diaphoresis)
151
Q

MC cause of transudative pleural effusions

A

CHF (left sided)

152
Q

Clinical manifestations of right sided HF

A
  • *Increase systemic venous pressure–> signs of systemic fluid retention
    1. Peripheral edema
    2. Increased JVP/jugular venous distention
    3. GI/Hepatic congestion- hepatosplenomegaly, anorexia
153
Q

How do you diagnose HF

A
  1. Echo** (measures LV function and EF)
  2. CXR: esp. for congestive HF
  3. Increased BNP: ventricles release BNP during volume overload
154
Q

What is the most important determinant of prognosis for HF

A

EF

155
Q

What is a normal and abnormal EF

A

Normal: 55-60%

EF less than 35%: increased mortality, Needs a cardioverter defibrillator in place to reduce mortality

156
Q

What is the initial management of HF

A
  1. ACEI (1st line in HF) + diuretic (for sx)
  2. Add BB
  3. Add Hydralazine + NTG
  4. Digoxin (add earlier if Afib)

*ACEI>BB best 2 drugs for decreased mortality

157
Q

Lifestyle changes to help manage HF

A
  1. Salt restriction <2g/d
  2. Fluid restriction <2L/d
  3. exercise
  4. smoking cessation
158
Q

HF meds to decrease afterload

A
  • vasodilators
    1. ACEI
    2. ARBs
    3. BB
    4. Hydralazine + Nitrates combo
159
Q

SE of ACEI

A
  1. hypotension
  2. Renal insufficiency
  3. hyperkalemia
  4. cough and angioedema (due to increased bradykinin)

*CI in pregnancy

160
Q

HF meds that decrease preload

A
  1. Diuretics
  2. HCTZ
  3. Metolazone
161
Q

What are loop diuretics

A
  1. furosemide
  2. bumetanide
  3. torsemide
162
Q

What type of diuretic is most effective tx for sx for mild-moderate CHF

A

loop diuretics

163
Q

SE of loop diuretics

A
  1. volume depletion
  2. hypOkalemia
  3. hypOcalcemia
  4. hypOnatremia
  5. HYPERglycemia
  6. HYPERuricemia
164
Q

SE of potassium sparing diuretics

A
  1. HYPERkalemia

2. gynecomastia w/ spironolactone

165
Q

___ diuretic is associated w/ decreased mortality and added in severe CHF

A

spironolactone

166
Q

Positive inotropes HF meds

A

(sympathomimetics)

  1. Digoxin
  2. Dobutamine
  3. Dopamine
167
Q

When is digoxin indicated

A

HF with Afib

*decrease hospitalizations and sx but NO mortality benefit w/ digoxin**

168
Q

What meds decrease mortality in HF

A
  1. ACEI
  2. ARBs
  3. BB
  4. Nitrates + hydralazine
  5. spironolactone
169
Q

___ meds are not generally sued in systolic HF

A

CCB

170
Q

what is congestive heart failure

A

acute decompensated HF w/ worsening of baseline sx, pulmonary congestion

171
Q

CXR findings of CHF

A
  1. Cephalization of vessels
  2. Kerley B lines (short linear markings at lung periphery)
  3. Peribronchial cuffing
  4. Cardiomegaly
  5. Perihilar congestion
172
Q

*Management of acute pulmonary edema/CHF

A

“LMNOP”

  • Lasix (removes fluid and relieves sx)
  • Morphine (decreases preload and heart strain)
  • Nitrates (venodilator that reduces preload and afterload)
  • Oxygen
  • Position (upright to decrease venous return)
173
Q

MC causes of pericarditis

A
  1. idiopathic (probably viral related)

2. Viral (enteroviruses, coxsackie, echovirus)

174
Q

Clinical manifestations of acute pericarditis

A

P’s

  1. Pleuritic CP (sharp and worse w/ inspiration)
  2. Persistent
  3. Postural (worse when supine and relieved w/ sitting or leaning forward)
  4. Pericardial friction rub (best heard at end expiration while upright and leaning forward
  5. +/- Fever
175
Q

EKG of pericarditis

A
  1. DIFFUSE ST elevations in precordial leads (CONCAVE up in V1-V6) and
  2. PR depressions

“Knuckle sign in AVR”- PR elevation w/ ST depression

176
Q

What is the use of echocardiogram in pericardititis

A

used to assess for complications of acute pericarditis (effusion or tamponade)

177
Q

Management of pericarditis

A
  • Anti-inflammatory drugs
    1. ASA or NSAIDS x 7-14 days (sx usually subside w/in 24hr)
    2. Colchicine is 2nd line management
    3. +/- Corticosteroids if sx >48hrs and refractory to 1st line meds

Dressler: ASA or colchicine

178
Q

Etiologies of pericardial effusion

A
  1. percarditits**
  2. Malignancy
  3. infection
179
Q

EKG of pericardial effusion

A

Low voltage QRS complex*

2. Electric alternans: cyclic beat to beat shift in QRS amplitude (tall QRS, short QRS…)(heart swinging in fluid)

180
Q

Tx of pericardial effusion

A
  1. Observe if smalla nd no evidence of tamponade
  2. tx underlying cause
  3. +/- pericardiocentesis if tamponade or large effusion
181
Q

What is pericardial tamponade

A

pericardial effusion causing significant pressure on the heart–> restriction of cardiac ventricular filling–> decreased cardiac output

182
Q

Clinical manifestations of pericardial tamponade

A
  1. Becks Triad
    - Distant (muffled heart sounds)
    - Increased JVP
    - systemic HYPOtension
  2. Pulsus paradoxus
  3. dyspnea
183
Q

What is pulsus paradoxus

A

exaggerated>10mmHg decrease in systolic BP w/ inspiration and pulses decrease w/ inspiration

184
Q

Echo: effusion + diastolic collapse of cardiac chambers

A

pericardial tamponade

185
Q

What is constrictive pericarditis

A

Thickened, fibrotic, calcified pericardium (from chronic pericarditits and inflammation) that restricts ventricular diastolic filling-> increases venous pressure and decreases stroke volume = decreased CO

186
Q

Clinical manifestations of constrictive pericardititis

A
  1. Dyspnea (MC SX)
  2. Right sided HF sx (increased JVD, peripheral edema)
  3. Kussmaul’s sign* (increased JVD during inspiration)
  4. pericardial knock*- high pitched 3rd heart sound due to sudden cessation of ventricular filling
187
Q

Management of constrictive pericarditits

A

pericardiectomy is definitive tx*

-diuretics may be used for symptomatic control

188
Q

What is the gold standard in diagnosing myocarditis

A

Endomyocardial biopsy–> commonly shows infiltration of lymphocytes with myocardial tissue necrosis

189
Q

Types of cardiomyopathies

A
  1. Dilated (95%)
  2. Restrictive (1%)
  3. Hypertrophic (HCMP 4%)
190
Q

MC cause of restrictive cardiomyopathy

A

amyloidosis (infiltrative dz)

191
Q

PE of hypertrophic cardiomyopathy

A
  1. Harsh Systolic cres-decresc murmurm at LLSB (sounds like AS)
  2. decrease murmur intensity by: increase venous return (squatting supine, handgrip)
  3. increase murmur intensity: decrease venous return (valsalva, standing, exertion, amyl nitrate)
  4. NO carotid radation
192
Q

What cardiomyopathy?
Echo: Marked dilation of both atria
-diastolic dysfunction

A

Restrictive cardiomyopathy

193
Q

What cardiomyopathy?

Echo: asymmetric wall thickness (esp septal)

A

Hypertrophic cardiomyopathy

194
Q

Management of Cardiomyopathies

  1. Dilated:
  2. Restrictive:
  3. Hypertrophic:
A
  1. Dilated: SHF tx, ACEI, diuretics
  2. Restrictive: tx underlying cause
  3. Hypertrophic: BB**, myomectomy, ETOH ablation
    * cautious use of digoxin nitrates and diuretics
195
Q

Acute autoimmune inflammatory multi-systemic illness mainly affecting children 5-15y/o

A

Rheumatic fever

196
Q

MC cause of rheumatic fever

A

1 .GABHS Group A B-hemolytic streptococcus (aka strep pyogenes)

197
Q

Complications of rheumatic fever

A
  1. rheumatic valvular dz:
    mitral (75%)
    Aortic (30%)
    Tricuspid and pulmonic (5%)
198
Q

Criteria for Rheumatic Fever

A

2 Major or 1 Major + 2 minor
PLUS: supporting evdence of recent GAS infection

Major: JONES
Joint (migratory polyarthritis)
Oh my heart (active carditits)
Nodules (subcutaneous)
Erythema marginatum
Sydenhams chorea

Minor:

  1. Fever 101.3 or 38.5
  2. Arthraglia (joint pain)
  3. Increase ESR, CRP, leukocytosis
  4. ECG: prolonged PR interval
199
Q

Tx of rheumatic fever

A
  1. ASA 2-6 weeks w/ taper +/- corticosteroids in severe cases
  2. Penicillin G antibiotic of choice (or Erythromycin in PCN allergic)

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